The hypothesis for a role of viral infections on the pathogenesis of systemic lupus erythematosus has been discussed in many works, particularly that of cytomegalovirus and Epstein Barr virus infections as trigger of autoimmune processes. Here, we describe the case of a young woman affected by systemic lupus erythematosus with marked hepatic involvement presenting IgM antibodies against cytomegalovirus, herpesvirus and herpes zoster virus in the absence of virus. The meaning of these laboratory findings is discussed.

Hereditary haemochromatosis is an autosomal recessive disorder of iron regulation that results in abnormal intestinal iron absorption with progressive iron overloading of parenchymal cells. Two specific, single point mutations of the HFE gene (C282Y and H63D) have been described in haemochromatosis patients. Epidemiological studies have revealed a strict association between hereditary haemochromatosis and C282Y homozygosis or C282Y/H63D compound heterozygosis, suggesting that these mutations may provide a useful tool for diagnosis. However, recent investigations from southern Europe have reported lower allelic frequencies of the C282Y mutation among haemochromatosis patients, apparently depending on the geographical area of the population analysed. To assess the predictive value of the detection of the C282Y and H63D HFE mutations in our geographical area, we have evaluated their occurrence in 46 haemochromatosis patients from southern Italy. We found that only 19.6% of our patients were homozygous for the C282Y mutation and 21.7% were compound C282Y/H63D heterozygotes. Among the remaining 59%, approximately 40% did not display any of the known HFE mutations. We conclude that, in southern Italy, another genetic determinant/s must be responsible for many haemochromatosis cases and that a genetic screening for the C282Y and H63D HFE mutations is not sufficient for hereditary haemochromatosis diagnosis.

Spleen size was assessed in 73 patients with thrombocytosis and in 15 healthy subjects, comparing palpation with ultrasonography (US) measurement of longitudinal diameter and volume. Intraobserver and interobserver variability for volume on US, checked in 12 patients, was very low. Correlation between spleen volume measured by US and that measured by computed tomography was excellent. Splenomegaly was detected by palpation in 25% of patients, by US assessment of longitudinal diameter in 33%, and by US assessment of volume in 52%. After diagnostic work-up, 54 patients had a diagnosis of essential thrombocythemia (ET), 4 of idiopathic myelofibrosis (IMF), and 15 of secondary thrombocytosis (ST). Spleen volume in patients with ST was in the normal range (138 +/- 47 mL) and was significantly lower than that in patients with ET or IMF (370 +/- 210 mL; P <.001). Thus, US-measured volume was the most sensitive method for identifying nonpalpable splenomegaly in patients with primary myeloproliferative diseases, and it may help in distinguishing these diseases from reactive disorders.

In immunocompromized hosts, febrile episodes have an unknown origin (FUO) in about fifty per cent of cases. In this preliminary study we evaluated the role of abdominal and pleural ultrasound (US) examination for early detection of infectious sites. US exploration was performed in a cohort of 14 consecutive FUO patients early after fever onset, at patients' bedside, by a hematologist trained in diagnostic ultrasound, and it was repeated at neutrophil recovery. US exploration showed abnormal abdominal findings in 7 and pleural effusion in 3 patients. In all cases but one the abnormality was found at the first US examination. Abdominal and pleural US exploration is a low-cost, easy to use tool for the work-up of FUO in the immunocompromized host that proved to be effective in identifying the infection site in about 50% of patients.